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1 tic approaches to neurocristopathies such as Hirschsprung's disease.
2  understanding newer therapeutic options for Hirschsprung's disease.
3 olons, and premature death, resembling human Hirschsprung's disease.
4 cristopathies, Waardenburg-Shah syndrome and Hirschsprung's disease.
5 ll migration have been shown to give rise to Hirschsprung's disease.
6 tive colitis, familial colonic polyposis, or Hirschsprung's disease.
7 lial medullary thyroid carcinoma (FMTC), and Hirschsprung's disease.
8 entiation, together with features typical of Hirschsprung's disease (aganglionic colon).
9 n colon samples from pediatric patients with Hirschsprung's disease and patients with chronic pseudo
10 nd mice, mutations in the Ret gene result in Hirschsprung's disease and renal defects.
11 ntrast, a RET mutant found in a patient with Hirschsprung's disease, as well as a RET/PTC1 mutant wit
12                 A one-stage pull-through for Hirschsprung's disease avoids the additional anesthesia,
13 es to the treatment of congenital megacolon (Hirschsprung's disease) based on the colonisation of the
14 ng leads to aganglionosis of the distal gut (Hirschsprung's disease), but it is unclear whether it is
15 stigate the cellular and molecular basis for Hirschsprung's disease caused by a mutation in the gene
16                 Recent trends in surgery for Hirschsprung's disease have been toward earlier repair a
17  addition, some patients with MEN 2A develop Hirschsprung's disease (HD), and all patients with MEN 2
18 entification of gold-standard treatments for Hirschsprung's Disease(HD) and gastroschisis.
19                                              Hirschsprung's disease (HSCR) causes functional intestin
20                                              Hirschsprung's disease (HSCR) is a severe congenital ano
21 rom variable lengths of the colon results in Hirschsprung's disease (HSCR) or colonic aganglionosis.
22 nd results in a condition in humans known as Hirschsprung's disease (HSCR).
23 vous system (ENS) development is relevant to Hirschsprung's disease (HSCR; congenital aganglionosis o
24 e lack of ganglia in the terminal hindgut of Hirschsprung's disease in humans or aganglionic megacolo
25 nesis of the inhibitory neurotransmission in Hirschsprung's disease in the distal colon and IAS.
26                          The pathogenesis of Hirschsprung's disease is not well understood.
27 s with defective migration of NCC that model Hirschsprung's disease, leading us to hypothesize that t
28 , anorectal malformations in 24 (47.1%), and Hirschsprung's disease, necrotising enterocolitis, and v
29 additional candidate genes that could modify Hirschsprung's disease penetrance.
30 hogenesis of inhibitory neurotransmission in Hirschsprung's disease was investigated.
31 usly shown to have a role in the etiology of Hirschsprung's disease, was misregulated within the gut
32  We report a 25-year-old woman with CCHS (no Hirschsprung's disease) who gave birth to a daughter who
33 s of a complex developmental anomaly such as Hirschsprung's disease will rely on unravelling its path
34 infectious diarrhea with zinc; achalasia and Hirschsprung's disease with botulinum toxin; weight loss
35 ced enteric nervous system characteristic of Hirschsprung's disease with reduced pigment cell number,

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